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J. Biol. Chem., Vol. 276, Issue 11, 7943-7951, March 16, 2001
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§,
, and
From the Cold shock domain (CSD) family members have been
shown to play roles in either transcriptional activation or repression
of many genes in various cell types. We have previously shown that CSD
proteins dbpAv and dbpB (also known as YB-1) act to repress granulocyte-macrophage colony-stimulating factor transcription in human
embryonic lung (HEL) fibroblasts via binding to single-stranded DNA
regions across the promoter. Here we show that the same CSD factors are
involved in granulocyte-macrophage colony-stimulating factor
transcriptional activation in Jurkat T cells. Unlike the mechanisms of
CSD repression in HEL fibroblasts, CSD-mediated activation in Jurkat T
cells is not mediated through DNA binding but presumably through
protein-protein interactions via the C terminus of the CSD protein with
transcription factors such as RelA/NF-
Division of Human Immunology, Hanson Centre
for Cancer Research, Institute of Medical and Veterinary Science, Frome
Road, Adelaide, South Australia, 5000 and the ¶ Division of
Biochemistry and Molecular Biology, John Curtin School of Medical
Research, Australian National University,
Canberra, Australian Capital Territory 2601, Australia
B p65. We demonstrate that
Jurkat T cells lack truncated CSD factor subtypes present in HEL
fibroblasts, which raises the possibility that the cellular content of
CSD proteins may determine their final role as activators or repressors
of transcription.
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